Abstract 262: Consumptive Coagulation in a Porcine Model of Prolonged Out-of-hospital Cardiac Arrest Treated with ECPR

Abstract

Background: Following prolonged cardiac arrest treated with extracorporeal cardiopulmonary resuscitation (ECPR), recovery of organ function and survival are potentially impaired due to a “no reflow” phenomenon associated with microvascular thrombosis. This study evaluated the effects of antithrombotic interventions on coagulation parameters in a in a porcine model of out-of-hospital cardiac arrest (OHCA). Hypothesis: We hypothesized that anticoagulant therapy (argatroban) during CPR and/or thrombolytic (streptokinase) therapy at onset of ECPR would prevent consumptive coagulopathy after prolonged cardiac arrest. Methods: In a blinded and randomized study, 48 swine (40±5kg) were subjected to 8min of ventricular fibrillation cardiac arrest followed by 30min of goal-directed CPR (gdCPR), and 8hr of ECPR (33°C) with heparin anticoagulation during ECPR titrated to ACT values (200-300s). Animals were randomized to one of 4 groups (n=12) with 350mg/kg argatroban (Arg) or placebo (20mL NSS) administered 12min after arrest and 1.5 MU streptokinase (STK) or placebo (50mL NSS) at ECPR initiation: Group 1 (placebo and placebo); Group 2 (Arg and placebo); Group 3 (placebo and STK); and Group 4 (Arg and STK). Blood samples were drawn at baseline and at 8hr of ECPR (or earlier if the experiment ended). Data was analyzed using t-tests and ANOVA (p<0.05 significant). Results: Average platelet count and fibrinogen levels significantly decreased between baseline and at the end of ECPR ( p =<0.0001) without difference between groups ( p =0.6315 and p =0.7692, respectively). D-dimer levels significantly increased across groups from baseline to the end of ECPR ( p =<0.0001) without difference between groups ( p =0.1881). Discussion: These results indicate that this OHCA model induces consumptive coagulopathy and the effects of antithrombotic therapies did not mitigate it in this porcine model.